As we age, we gradually accumulate damage to our DNA. The link between DNA damage and cancer is well established, but there is growing evidence of a contribution to other diseases, including cardiovascular disease and inflammatory disorders. This project aims to accelerate the natural decay of the genome to determine how somatic mutations contribute to ageing and how this triggers disease.
Genetic engineering will be used to manipulate DNA repair pathways. We will stimulate diverse forms of DNA damage and track their influence on clonal expansions and disease risk. Using these models we will study how real-world stresses, like cancer therapy, chronic inflammation or infections modify patterns of clonal selection.
Our research investigates why cancers develop and how they change in response to therapy. Our primary strengths are in cancer genetics and genomics, with an emphasis on DNA repair. We use genomic approaches to study the genetic and transcriptional landscape of cancer, then we model these alterations to determine precisely how they work.
This project builds on preliminary studies performed in our lab that have tracked different patterns of DNA damage in human cancers. The project will appeal to students who want to gain expertise in cancer biology, haematology, genomics and molecular biology.
These papers help illustrate the type of work that we do: